4.6 Article

Production of steroids by human ovarian surface epithelial cells in culture:: Possible role of progesterone as growth inhibitor

期刊

GYNECOLOGIC ONCOLOGY
卷 82, 期 1, 页码 116-121

出版社

ACADEMIC PRESS INC
DOI: 10.1006/gyno.2001.6219

关键词

ovarian surface epithelium; progesterone; estradiol; proliferation

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Objective. The purpose was to investigate whether normal ovarian surface epithelial cells, harvested from premenopausal and postmenopausal women, are capable of steroid production, and to evaluate effects of estradiol and progesterone on growth regulation of such cells. Methods. Ovarian surface epithelial cells were obtained by brushing of the ovarian surface of 9 premenopausal and 10 postmenopausal women undergoing surgery for benign gynecological diseases. The conditioned media after culture, with and without addition of FSH and LH, were analyzed for estradiol and progesterone. The proliferative effects of the steroids were analyzed using two different culture models, nonconfluent cells and confluent cells, and two different detection methods, [H-3]thymidine incorporation and a colorimetric method assaying cell number. Results. The normal ovarian surface epithelial cells were found to secrete both estradiol and progesterone, a production that was not regulated by FSH or LH. Addition of steroids to the cultured cells did not induce any overall significant growth effects. However, progesterone significantly inhibited the growth of ovarian surface epithelial cells from three of the patients. Enhanced thymidine incorporation was observed in the presence of the progesterone receptor antagonist Org 31710 in the nonconfluent cultures of cells from postmenopausal women, but no effect of an estrogen receptor antagonist was observed. Conclusions. The normal ovarian surface epithelium is capable of steroid production, which is also often observed in tissue from ovarian epithelial tumors. Progesterone appeared to be a negative regulator of ovarian surface epithelial growth, while estradiol had no effect. (C) 2001 Academic Press.

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